Objective To summarize the papers about the research status and prospects of ferroptosis in hepatocellular carcinoma (HCC) and its drug resistance in recent years in order to provide directions and ideas for the treatment of HCC. Method The relevant literatures at home and abroad in recent years about ferroptosis in HCC and its drug resistance were reviewed. Results The mechanism of ferroptosis in the development and drug resistance of HCC was complicated, involving multiple protein and molecular pathways. Ferroptosis played an important role in improving chemotherapy and sorafenib resistance, and it had a broad application prospect in HCC. Conclusions The molecular mechanism of ferroptosis in HCC and its drug resistance has not been fully elucidated. Further research on the mechanism of ferroptosis in HCC may provide new molecular therapeutic targets for HCC. Ferroptosis has a broad application prospect in the treatment of HCC.
Objective To summarize the clinical significance of endoscopic treatment for obstructive jaundice. Methods The recently published literatures in domestic and abroad about endoscopic treatment for obstructive jaundice were reviewed. Results The results of endoscopic treatment for bile duct stones and bile duct surgery for biliary stricture had the same outcome. The endoscopic treatment could identify bile duct and duodenal periampullary tumors and lesions. Conclusion Endoscopic treatment for obstructive jaundice is a safe and effective method.
Objective To investigate the expression of tumor suppressor gene Lumican mRNA in gastric cancer and its role in the development of gastric cancer. Methods The expressions of Lumican mRNA in gastric cancer tissues, tissues near tumor and normal tissues were detected by using reverse transcription polymerase chain reaction (RT-PCR), clinical pathology for those tissues was studied as well. Results The expression absence rates of Lumican mRNA were 42.4% (28/66), 15.2% (10/66) and 0 in gastric cancer tissues, tissues near tumor and normal tissues respectively. The expression absence rate of Lumican mRNA in patients with lymph node metastasis was 61.1%, which was significantly higher than that of the patients without lymph node metastasis (20.0%, χ2=11.323, P=0.001). The expression absence rate of Lumican mRNA in the gastric cancer at the advanced stages (stages Ⅲ, Ⅳ) was 61.5%, which was significantly higher than that in the gastric cancer at the early stages (stages Ⅰ, Ⅱ, 30.0%, χ2=6.417， P=0.011). The expression absence rates of Lumican mRNA in the high, moderate and poor differentiation tumors were 38.5% (10/26), 38.5% (10/26) and 57.1% (8/14) respectively, the expression absence rate of Lumican mRNA was no significant association with the differentiation degree (χ2=1.576, P=0.455). Conclusion The expression absence of tumor suppressor gene Lumican mRNA may play an important role in the tumorgenesis and influences the prognosis of gastric cancer.
Objective To investigate the risk factors, prevention and therapy of hepatic artery thrombosis after liver transplantation. Methods The literatures on the risk factors, prevention and therapy of hepatic artery thrombosis after liver transplantation in recent years were collected and reviewed. Results The risk factors include factor Ⅴ Leiden, metabolic liver diseases of recipients, recipient sex, the use of Roux-en-Y biliary reconstructions, virus infection and so on. The measures of prevention and therapy include early diagnosis, detection of activated protein C resistance, postoperative anti-coagulation therapy, liver arteries reconstructions measures, hyperbaric oxygen therapy, continuous transcatheter arterial thrombolysis, liver retransplantation and so on. Conclusion The study of risk factors, prevention and therapy will promote the process of improving the prognosis of patients with liver transplantation.
ObjectiveTo summarize the papers about the molecular mechanisms of liver metastasis from colorectal cancer in recent years and in order to provide assistance for the diagnosis and treatment of liver metastases from colorectal cancer.MethodThe relevant literatures at home and abroad in recent years about the molecular mechanisms of liver metastasis from colorectal cancer were reviewed.ResultsThe molecular mechanism of liver metastasis from colorectal cancer is complicated. For example, microRNA-192 could inhibit liver metastasis from colorectal cancer through multiple targets, however microRNA-181a could promote liver metastasis from colorectal cancer. TGF-β inhibits liver metastasis from colorectal cancer by inhibiting cell proliferation and Smad-dependent signaling to induce apoptosis. Elevated CEA level not only help in the diagnosis of colorectal cancer, but also as a prognostic indicator for colorectal cancer patients. CEA could promote liver metastasis by affecting the survival of colorectal cancer cells in vessels, changeing the liver microenvironment, and affecting the adhesion and survival of circulating tumor cells in the liver.ConclusionsThe molecular mechanism of liver metastasis of colorectal cancer has not been fully elucidated. Through in-depth study of the mechanism of liver metastasis of colorectal cancer, it can provide molecular targets for targeted therapy in patients with liver metastases from colorectal cancer, such as bevacizumab, cetuximab, panitumab and so on. Detecting the change of serological markers in patients with colorectal cancer can help diagnose, judge recurrence, prognosis and metastasis.
Objective To observe the outcomes of using different concentrations of arsenic trioxide at varying phases on the breast cancer cell line MCF-7 and to study the mechanism of this effect. Methods The effect of arsenic trioxide on the growth of breast cancer cell line MCF-7 was observed after applying arsenic trioxide of different concentrations （0.5-16 μmol/Ｌ）. The inhibitory effect of arsenic trioxide on the cell proliferation was investigated with 3-(4，5-dimethyl-thizazol-2-yl)-2， 5-diphenyl tetrazolium bromide (MTT) and the induction of arsenic trioxide on cell apoptosis was detected by DNA ladder and terminal deoxynucleotidyl transferase mediated nick end labeling (TUNEL). Results The effect of arsenic trioxide on breast cancer cell line MCF-7 depended on the phase and the dose. The number of cell decreased significantly and there were conspicuously typical morphological changes of apoptosis after the use of arsenic trioxide， including membrane blebbing， chromatin pyknosis, nuclear fragmentation and the formation of apoptotic body. The typical DNA ladders were observed in the MCF-7 cells after 48 h administration of arsenic trioxide at concentrations 1-8 μmol/Ｌ. Significant elevations of apoptosis index at 24 h, 48 h and 72 h were all detected by TUNEL after incubating with 4 μmol/L arsenic trioxide. Conclusion Arsenic trioxide may inhibit the growth of breast cancer cell line MCF-7 significantly by inducing the apoptosis of breast cancer cell.